ReviewCurrent opinion in organ transplantation2009
Innate immunity in heart transplantation.
Review in Current opinion in organ transplantation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Toll-like receptors and damage-associated molecular patterns in the pathogenesis of heart transplant rejection.Molecular and cellular biochemistry · 2022Review
- Significant role for microRNA-21 affecting toll-like receptor pathway in primary graft dysfunction after human lung transplantation.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2017Article
- Role of Mitogen-Activated Protein Kinases in Myocardial Ischemia-Reperfusion Injury during Heart Transplantation.Journal of transplantation · 2012Article
- Elevated plasma long pentraxin-3 levels and primary graft dysfunction after lung transplantation for idiopathic pulmonary fibrosis.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2011Article
- Early innate immune events induced by prolonged cold ischemia exacerbate allograft vasculopathy.Journal of cardiothoracic surgery · 2011Article
- Neutrophil mediated smooth muscle cell loss precedes allograft vasculopathy.Journal of cardiothoracic surgery · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purpose of reviewCardiac transplantation is the treatment of choice for end-stage heart failure, but its efficacy is limited by the development of cardiac allograft vasculopathy (CAV). Although the adaptive immune system is efficiently suppressed by conventional drugs, the innate immune system is largely unaffected. The innate response may contribute both to stimulation of the adaptive response and to the future development of CAV. RECENT
findingsStimulation of Toll-like receptors by endogenous ligands released in response to ischemia/reperfusion causes an inflammatory milieu favorable to graft rejection and unfavorable to tolerance. New evidence suggests that natural killer cells have previously unknown memory-like features and are capable of graft rejection. Their role in rejecting the cardiac allograft has previously been underestimated. Complement deposition may also contribute to acute cellular rejection and CAV. SUMMARY: The innate immune system is an important but neglected component of allograft rejection. Drugs that target Toll-like receptors, natural killer cells and complement may play an important role in preventing CAV and achieving tolerance to cardiac allografts.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.